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      A Case of COVID-19 in a Patient with Asymptomatic Hemoglobin D Thalassemia and Glucose-6-Phosphate Dehydrogenase Deficiency

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          Abstract

          Patient: Gender, 26-year-old

          Final Diagnosis: COVID-19

          Symptoms: Cough • fever

          Medication:—

          Clinical Procedure: —

          Specialty: Hematology

          Objective:

          Rare co-existance of disease or pathology

          Background:

          Beta-hemoglobinopathies and glucose-6-phosphate dehydrogenase (G6PD) deficiency are genetic disorders that cause hemolytic anemia when exposed to oxidative stress. Their co-existence is, however, not proven to enhance the severity of anemia.

          Case Report:

          We report the case of a young man with no known co-morbidities, who came with fever and cough and was diagnosed with COVID-19 pneumonia. He was found to have hemoglobin D thalassemia and G6PD deficiency during further evaluation. Hydroxychloroquine therapy started initially, was discontinued after 3 doses once the G6PD deficiency was diagnosed. His hospital course showed a mild drop in hemoglobin with evidence of hemolysis on peripheral smear. However, the hemoglobin improved without any need for transfusion.

          Conclusions:

          Hydroxychloroquine therapy can induce hemolytic crises in patients with underlying G6PD deficiency or hemoglobinopathies and should be avoided or closely monitored. Immediate intervention to stop hydroxychloroquine after 3 doses saved our patient from a major hemolytic crisis. The significance of this case report is that it is the first report that outlines the clinic course of COVID-19 pneumonia in a patient with underlying hemoglobin D disease and G6PD deficiency.

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          Most cited references12

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          Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial

          Background Chloroquine and hydroxychloroquine have been found to be efficient on SARS-CoV-2, and reported to be efficient in Chinese COV-19 patients. We evaluate the role of hydroxychloroquine on respiratory viral loads. Patients and methods French Confirmed COVID-19 patients were included in a single arm protocol from early March to March 16th, to receive 600mg of hydroxychloroquine daily and their viral load in nasopharyngeal swabs was tested daily in a hospital setting. Depending on their clinical presentation, azithromycin was added to the treatment. Untreated patients from another center and cases refusing the protocol were included as negative controls. Presence and absence of virus at Day6-post inclusion was considered the end point. Results Six patients were asymptomatic, 22 had upper respiratory tract infection symptoms and eight had lower respiratory tract infection symptoms. Twenty cases were treated in this study and showed a significant reduction of the viral carriage at D6-post inclusion compared to controls, and much lower average carrying duration than reported of untreated patients in the literature. Azithromycin added to hydroxychloroquine was significantly more efficient for virus elimination. Conclusion Despite its small sample size our survey shows that hydroxychloroquine treatment is significantly associated with viral load reduction/disappearance in COVID-19 patients and its effect is reinforced by azithromycin.
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            Coronavirus Disease 2019: Coronaviruses and Blood Safety

            With the outbreak of unknown pneumonia in Wuhan, China, in December 2019, a new coronavirus, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), aroused the attention of the entire world. The current outbreak of infections with SARS-CoV-2 is termed Coronavirus Disease 2019 (COVID-19). The World Health Organization declared COVID-19 in China as a Public Health Emergency of International Concern. Two other coronavirus infections—SARS in 2002-2003 and Middle East Respiratory Syndrome (MERS) in 2012—both caused severe respiratory syndrome in humans. All 3 of these emerging infectious diseases leading to a global spread are caused by β-coronaviruses. Although coronaviruses usually infect the upper or lower respiratory tract, viral shedding in plasma or serum is common. Therefore, there is still a theoretical risk of transmission of coronaviruses through the transfusion of labile blood products. Because more and more asymptomatic infections are being found among COVID-19 cases, considerations of blood safety and coronaviruses have arisen especially in endemic areas. In this review, we detail current evidence and understanding of the transmission of SARS-CoV, MERS–CoV, and SARS-CoV-2 through blood products as of February 10, 2020, and also discuss pathogen inactivation methods on coronaviruses.
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              Glucose-6-Phosphate Dehydrogenase Deficiency Enhances Human Coronavirus 229E Infection

              Abstract The host cellular environment is a key determinant of pathogen infectivity. Viral gene expression and viral particle production of glucose-6-phosphate dehydrogenase (G6PD)–deficient and G6PD-knockdown cells were much higher than their counterparts when human coronavirus (HCoV) 229E was applied at 0.1 multiplicity of infection. These phenomena were correlated with increased oxidant production. Accordingly, ectopic expression of G6PD in G6PD-deficient cells or addition of antioxidant (such as α-lipoic acid) to G6PD-knockdown cells attenuated the increased susceptibility to HCoV 229E infection. All experimental data indicated that oxidative stress in host cells is an important factor in HCoV 229E infectivity
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                Author and article information

                Journal
                Am J Case Rep
                Am J Case Rep
                amjcaserep
                The American Journal of Case Reports
                International Scientific Literature, Inc.
                1941-5923
                2020
                22 July 2020
                : 21
                : e925788-1-e925788-6
                Affiliations
                [1 ]Department of Internal Medicine, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar
                [2 ]Department of Hematology, National Centre for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar
                [3 ]Department of Infectious Diseases, Communicable Disease Center, Hamad Medical Corporation, Doha, Qatar
                Author notes
                Corresponding Author: Sreethish Sasi, e-mail: Ssasi7@ 123456hamad.qa

                Authors’ Contribution:

                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                Conflict of interest: None declared

                Source of support: Qatar National Library

                Article
                925788
                10.12659/AJCR.925788
                7394553
                32697769
                bdbcde56-ba8e-4be3-b31a-a529582a353e
                © Am J Case Rep, 2020

                This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International ( CC BY-NC-ND 4.0)

                History
                : 08 May 2020
                : 03 June 2020
                : 22 June 2020
                Categories
                Articles

                covid-19,glucosephosphate dehydrogenase deficiency,hemoglobinopathies,hydroxychloroquine,sars virus

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